Dr  Muhammad Fairuz Jamaluddin

Dr Muhammad Fairuz Jamaluddin

Associate Lecturer

School of Biomedical Sciences and Pharmacy

Career Summary

Biography

Dr Fairuz Jamaluddin is an Associate Lecturer and Postdoctoral researcher who is developing expertise in gynaecology oncology. He was awarded with John Hunter Hospital Charitable Trust project grant (3x) since 2017 to advance his project. He independently pursued his own research project on the molecular basis of uterine fibroids, ovarian cancer and endometrial cancer, combining human genetics and mass spectrometry-based proteomics.

Dr Fairuz Jamaluddin graduated his PhD in 2015 at the University of Queensland. During his doctoral studies, he learnt and developed new methodologies in glycoproteomics in Associate Professor Benjamin Schulz’s lab. In 2016, he joined the Gynaecology Oncology Research Group of Professor Pradeep Tanwar (NHMRC fellow and international leader on gynaecological cancer research) as a Postdoctoral Researcher in the School of Biomedical Sciences and Pharmacy, University of Newcastle.  Dr Jamaluddin has published in high impact journals including PNAS x2, Molecular and Cellular Proteomics x2, Nature Communications x2Cell Reports Medicine and Protein Science; including 10 first author in Research article papers. In particular, his work with Prof Tanwar is the first study in the field to characterise the matrisome of uterine fibroids and identified the key biomarkers of this disease development in genetically annotated patient samples (Endocrinology 2018). This work led to ‘Publication of the Month May 2018’ awarded by the School of Biomedical Science and Pharmacy. Dr Jamaluddin pioneering work also identified two novel ECM proteins namely periostin (Endocrinology 2018) and tenascin-C (Reproductive Science 2019) that are upregulated in fibroid patients. He is also one of the co-authors involved in investigating the mechanistic insight how changes in ECM and its biomechanical properties leads to overactivation of canonical Wnt/β-catenin signalling (Reproduction 2018). Based on his outstanding contributions to the field, he was awarded with ‘Kellerman Award 2019’ by the Faculty of Health and Medicine.

Research Focus

Dr Fairuz Jamaluddin research is focused on discovering new ways of detecting and treating diseases of the female reproductive tract including endometriosis, fibroids, ovarian cancer and endometrial cancer. Dr Jamaluddin is interested in applying mass spectrometry-based proteomics as a powerful tool to study protein profiles of diseased and normal tissues. By comparing protein profiles of diseased and normal tissues, new protein biomarkers for early diagnosis or developing new drug treatments can be uncovered.

His current research addresses three main areas:

- Targeting extracellular matrix as therapeutic approach in uterine leiomyoma (fibroids)

- New drug targets for ovarian cancer metastasis and drug resistance

- Disease biomarkers for early detection of endometriosis and endometrial cancer


Qualifications

  • Doctor of Philosophy, University of Queensland

Keywords

  • Extracellular matrix
  • Medical Biochemistry
  • Proteomics

Languages

  • English (Fluent)
  • Malay (Mother)

Professional Experience

UON Appointment

Title Organisation / Department
Associate Lecturer University of Newcastle
School of Biomedical Sciences and Pharmacy
Australia

Academic appointment

Dates Title Organisation / Department
1/2/2017 - 31/1/2018 Lecturer School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
Australia

Awards

Award

Year Award
2023 CDT EMCR Awards 2023: Best Publication Award - 1st place
Hunter Medical Research Institute (HMRI)
2019 The Kellerman Award
Faculty of Health and Medicine, University of Newcastle

Prize

Year Award
2018 Publication of the Month May
Faculty of Health and Medicine, University of Newcastle

Thesis Examinations

Year Level Discipline Thesis
2019 Honours Health Immune profiling in primary and recurrent glioblastoma tumors and peripheral blood

Teaching

Code Course Role Duration
HUBS3409 Projects in Biomedical Science
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle

This course provide an opportunity for students to study a current field of research in biomedical science in greater depth and to gain the intellectual and professional skills associated with managing, implementing and reporting on a biomedical research project. The assessment on student performance in this course is based on their literature review, project seminar, project manuscript and supervisors report.

Teaching 1/2/2017 - 31/1/2018
MEDI2101B Clinical Sciences, Scholarship and Practice 2 Part B (MEDI2101B)
School of Medicine & Public Health, Faculty of Health & Medicine, University of Newcastle | Australia

This course builds on foundational skills and knowledge gained in MEDI1101 to examine specific content related to endocrinology; the musculoskeletal and nervous systems; ear, nose and throat; ophthalmology; reproduction; emotion and behaviour; clinical haematology; chemistry; immunology; microbiology; genetics and cell pathology.

The course presents students with a series of problem based learning (PBL) scenarios in order to further develop students’ knowledge and skills for clinical practice. PBL scenarios are used to drive student learning and begin the student’s integration of the sciences that inform medical practice. PBL content continues to be presented using the organising framework of the extended family and their experiences of health, illness and medicine.

Skills that are related to clinical practice are taught and assessed throughout the course using simulation and clinical placement experiences. Students apply more complex knowledge of pharmacotherapeutics to management of the patient with conditions related to the above. Students apply the concept of diagnostics through the integration of history taking, physical examination and use of appropriate, readily available diagnostic tests.

Elements of the course have a particular focus on the elements of medical practice related to the role of doctors as advocates for the health and wellbeing of individuals and communities.

Facilitator 13/7/2022 - 10/11/2022
HUBS2206 Human Biochemistry and Cell Biology
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
This course provides students with knowledge and understanding of the structure and function of the cells with an emphasis on molecular aspects. It involves integrated learning between the areas of Biochemistry and Molecular Biology. Practical sessions develop core skills that prepare students for a career in laboratory-based research in the biomedical sciences.
Lecturer 7/3/2022 - 23/5/2022
HUBS3412 Work Integrated Learning in Biomedical Science 1
School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle
This course is a research or industry placement course, which provides an opportunity for a student to work as part of a research laboratory, or within industry.
Examiner/Evaluator 19/7/2021 - 29/10/2021
MEDI2101A Clinical Sciences, Scholarship and Practice 2 Part A
College of Health, Medicine & Wellbeing - The University of Newcastle

This course builds on foundational skills and knowledge gained in MEDI1101 to examine specific content related to endocrinology; the musculoskeletal and nervous systems; ear, nose and throat; ophthalmology; reproduction; emotion and behaviour; clinical haematology; chemistry; immunology; microbiology; genetics and cell pathology. The course presents students with a series of problem based learning (PBL) scenarios in order to further develop students’ knowledge and skills for clinical practice. PBL scenarios are used to drive student learning and begin the student’s integration of the sciences that inform medical practice. PBL content continues to be presented using the organising framework of the extended family and their experiences of health, illness and medicine.

Skills that are related to clinical practice are taught and assessed throughout the course using simulation and clinical placement experiences. Students apply more complex knowledge of pharmacotherapeutics to management of the patient with conditions related to the above. Students apply the concept of diagnostics through the integration of history taking, physical examination and use of appropriate, readily available diagnostic tests. Elements of the course have a particular focus on the elements of medical practice related to the role of doctors as advocates for the health and wellbeing of individuals and communities.

Facilitator 17/2/2022 - 10/6/2022
Edit

Publications

For publications that are currently unpublished or in-press, details are shown in italics.

Highlighted Publications

Year Citation Altmetrics Link
2018 Jamaluddin MFB, Nahar P, Tanwar PS, 'Proteomic characterization of the extracellular matrix of human uterine fibroids', Endocrinology, 159 2656-2669 (2018) [C1]

Uterine leiomyomas (fibroids) are the most common benign tumors that are associated with increased production of extracellular matrix (ECM). Excessive ECM deposition plays a major... [more]

Uterine leiomyomas (fibroids) are the most common benign tumors that are associated with increased production of extracellular matrix (ECM). Excessive ECM deposition plays a major role in the enlargement and stiffness of these tumors and contributes to clinical symptoms, such as abnormal bleeding and abdominal pain. However, no study so far has explored the global composition of the ECM of fibroids and normal myometrium. In this study, we performed a systematic ECM enrichment procedure and comparative proteomic analyses to profile the ECM composition of genetically annotated different-sized fibroids (small, medium, and large) and adjacent normal myometrium (ANM). Our matrisome analysis identified a combined total of 108, 126, 126, and 130 unique ECM and ECM-associated proteins with a confidence corresponding to a false discovery rate,1%inANM and in small, medium, and large fibroids, respectively. The majority of fibroid ECM proteins belong to the core matrisome that includes glycoproteins, collagens, and proteoglycans. Considering that the small-sized fibroids represent the initial stages of leiomyogenesis, we highlighted some of the most abundant and important upregulated ECM proteins in small fibroids (i.e., POSTN, TNC, COL3A1, COL24A1, and ASPN). Furthermore, we revealed 30 unique ECM proteins that exist only in fibroids but that are not present in ANM regardless of MED12 mutation. We propose that some of the proteins identified represent potential novel ECM drug targets that may change the paradigm of fibroid treatment.

DOI 10.1210/en.2018-00151
Citations Scopus - 24Web of Science - 17
Co-authors Pradeep Tanwar
2018 Jamaluddin MFB, Ko YA, Kumar M, Brown Y, Bajwa P, Nagendra PB, et al., 'Proteomic profiling of human uterine fibroids reveals upregulation of the extracellular matrix protein periostin', Endocrinology, 159 1106-1118 (2018) [C1]

The central characteristic of uterine fibroids is excessive deposition of extracellular matrix (ECM), which contributes to fibroid growth and bulk-type symptoms. Despite this, ver... [more]

The central characteristic of uterine fibroids is excessive deposition of extracellular matrix (ECM), which contributes to fibroid growth and bulk-type symptoms. Despite this, very little is known about patterns of ECM protein expression in fibroids and whether these are influenced by the most common genetic anomalies, which relate to MED12. We performed extensive genetic and proteomic analyses of clinically annotated fibroids and adjacent normal myometrium to identify the composition and expression patterns of ECM proteins in MED12 mutation-positive and mutation-negative uterine fibroids. Genetic sequencing of tissue samples revealed MED12 alterations in 39 of 65 fibroids (60%) from 14 patients. Using isobaric tagged-based quantitative mass spectrometry on three selected patients (n = 9 fibroids), we observed a common set of upregulated (.1.5-fold) and downregulated (,0.66-fold) proteins in small, medium, and large fibroid samples of annotated MED12 status. These two sets of upregulated and downregulated proteins were the same in all patients, regardless of variations in fibroid size and MED12 status. We then focused on one of the significant upregulated ECM proteins and confirmed the differential expression of periostin using western blotting and immunohistochemical analysis. Our study defined the proteome of uterine fibroids and identified that increased ECM protein expression, in particular periostin, is a hallmark of uterine fibroids regardless of MED12 mutation status. This study sets the foundation for further investigations to analyze the mechanisms regulating ECM overexpression and the functional role of upregulated ECM proteins in leiomyogenesis.

DOI 10.1210/en.2017-03018
Citations Scopus - 16Web of Science - 11
Co-authors Pradeep Tanwar, David Skerrett-Byrne, Hubert Hondermarck, Mark Baker, Rodney Scott, Matt Dun
2019 Jamaluddin MFB, Nagendra PB, Nahar P, Oldmeadow C, Tanwar PS, 'Proteomic Analysis Identifies Tenascin-C Expression Is Upregulated in Uterine Fibroids', REPRODUCTIVE SCIENCES, 26 476-486 (2019) [C1]
DOI 10.1177/1933719118773420
Citations Scopus - 6Web of Science - 3
Co-authors Christopher Oldmeadow, Pradeep Tanwar
2022 Jamaluddin MFB, Ghosh A, Ingle A, Mohammed R, Ali A, Bahrami M, et al., 'Bovine and human endometrium-derived hydrogels support organoid culture from healthy and cancerous tissues', Proceedings of the National Academy of Sciences, 119 (2022) [C1]
DOI 10.1073/pnas.2208040119
Citations Scopus - 22Web of Science - 3
Co-authors Ayesha Ayesha, Arnab Ghosh, Zamira Gibb, Ajayan Vinu, Gerard Kaiko, Pradeep Tanwar
2022 Jamaluddin MFB, Ko Y-A, Ghosh A, Syed SM, Ius Y, O'Sullivan R, et al., 'Proteomic and functional characterization of intra-tumor heterogeneity in human endometrial cancer', CELL REPORTS MEDICINE, 3 (2022) [C1]
DOI 10.1016/j.xcrm.2022.100738
Citations Scopus - 7Web of Science - 5
Co-authors Shafiq Syed, Arnab Ghosh, Mark Baker, Pradeep Tanwar
2023 Jamaluddin MFB, Nagendra PB, Ko Y-A, Bajwa P, Scott RJ, Nahar P, Tanwar PS, 'Prevalence and clinical significance of co-existing mutations in MED12 and FH in uterine fibroids of Australian women', Frontiers in Reproductive Health, 5 [C1]
DOI 10.3389/frph.2023.1081092
Co-authors Pradeep Tanwar, Rodney Scott
2023 Jamaluddin MFB, Day T, Tanwar PS, Marzol A, Scurry J, 'Mass Spectrometry Proteomic Analysis of Four p53 Patterns in Differentiated Vulvar Intraepithelial Neoplasia.', J Low Genit Tract Dis, 27 146-151 (2023) [C1]
DOI 10.1097/LGT.0000000000000720
Co-authors Pradeep Tanwar

Chapter (1 outputs)

Year Citation Altmetrics Link
2019 Gould T, Jamaluddin M, Petit J, King SJ, Nixon B, Scott R, et al., 'Finding Needles in Haystacks: The Use of Quantitative Proteomics for the Early Detection of Colorectal Cancer', Advances in the Molecular Understanding of Colorectal Cancer, IntechOpen, Switzerland 1-32 (2019) [B1]
DOI 10.5772/intechopen.80942
Co-authors Rodney Scott, Brett Nixon, Peter Pockney, Matt Dun

Journal article (32 outputs)

Year Citation Altmetrics Link
2024 Duchatel RJ, Jackson ER, Parackal SG, Kiltschewskij D, Findlay IJ, Mannan A, et al., 'PI3K/mTOR is a therapeutically targetable genetic dependency in diffuse intrinsic pontine glioma.', J Clin Invest, 134 (2024) [C1]
DOI 10.1172/JCI170329
Citations Scopus - 1
Co-authors David Skerrett-Byrne, Susan Hua, Heather Murray, Murray Cairns, Matt Dun, Ryan Duchatel, Brett Nixon, Christopher Dayas, Lizzie Manning
2023 Jamaluddin MFB, Nagendra PB, Ko Y-A, Bajwa P, Scott RJ, Nahar P, Tanwar PS, 'Prevalence and clinical significance of co-existing mutations in MED12 and FH in uterine fibroids of Australian women', Frontiers in Reproductive Health, 5 [C1]
DOI 10.3389/frph.2023.1081092
Co-authors Pradeep Tanwar, Rodney Scott
2023 La T, Chen S, Zhao XH, Zhou S, Xu R, Teng L, et al., 'LncRNA LIMp27 Regulates the DNA Damage Response through p27 in p53-Defective Cancer Cells.', Adv Sci (Weinh), 10 e2204599 (2023) [C1]
DOI 10.1002/advs.202204599
Citations Scopus - 2
Co-authors Xiaohong Zhao, Xu Zhang, Yuchen Feng, Lei Jin, Yuanyuan Zhang
2023 Staudt DE, Murray HC, Skerrett-Byrne DA, Smith ND, Jamaluddin MFB, Kahl RGS, et al., 'Phospho-heavy-labeled-spiketide FAIMS stepped-CV DDA (pHASED) provides real-time phosphoproteomics data to aid in cancer drug selection (vol 19, 48, 2022)', CLINICAL PROTEOMICS, 20 (2023)
DOI 10.1186/s12014-023-09406-z
Co-authors Ryan Duchatel, Heather Murray, Matt Dun, David Skerrett-Byrne, Brett Nixon
2023 Jamaluddin MFB, Day T, Tanwar PS, Marzol A, Scurry J, 'Mass Spectrometry Proteomic Analysis of Four p53 Patterns in Differentiated Vulvar Intraepithelial Neoplasia.', J Low Genit Tract Dis, 27 146-151 (2023) [C1]
DOI 10.1097/LGT.0000000000000720
Co-authors Pradeep Tanwar
2023 Kumar M, Sahoo SS, Jamaluddin MFB, Tanwar PS, 'Loss of liver kinase B1 in human seminoma', Frontiers in Oncology, 13 (2023) [C1]

Testicular cancer is a common malignancy of young males and is believed to be originated from defective embryonic or adult germ cells. Liver kinase B1 (LKB1) is a serine/threonine... [more]

Testicular cancer is a common malignancy of young males and is believed to be originated from defective embryonic or adult germ cells. Liver kinase B1 (LKB1) is a serine/threonine kinase and a tumor suppressor gene. LKB1 is a negative regulator of the mammalian target of rapamycin (mTOR) pathway, often inactivated in many human cancer types. In this study, we investigated the involvement of LKB1 in the pathogenesis of testicular germ cell cancer. We performed immunodetection of LKB1 protein in human seminoma samples. A 3D culture model of human seminoma was developed from TCam-2 cells, and two mTOR inhibitors were tested for their efficacy against these cancer cells. Western blot and mTOR protein arrays were used to show that these inhibitors specifically target the mTOR pathway. Examination of LKB1 showed reduced expression in germ cell neoplasia in situ lesions and seminoma compared to adjacent normal-appearing seminiferous tubules where the expression of this protein was present in the majority of germ cell types. We developed a 3D culture model of seminoma using TCam-2 cells, which also showed reduced levels of LKB1 protein. Treatment of TCam-2 cells in 3D with two well-known mTOR inhibitors resulted in reduced proliferation and survival of TCam-2 cells. Overall, our results support that downregulation or loss of LKB1 marks the early stages of the pathogenesis of seminoma, and the suppression of downstream signaling to LKB1 might be an effective therapeutic strategy against this cancer type.

DOI 10.3389/fonc.2023.1081110
Co-authors Pradeep Tanwar
2022 Venkata VD, Jamaluddin MFB, Goad J, Drury HR, Tadros MA, Lim R, et al., 'Development and characterization of human fetal female reproductive tract organoids to understand Müllerian duct anomalies', Proceedings of the National Academy of Sciences of the United States of America, 119 (2022) [C1]

Müllerian ducts are paired tubular structures that give rise to most of the female repro- ductive organs. Any abnormalities in the development and differentiation of these ducts l... [more]

Müllerian ducts are paired tubular structures that give rise to most of the female repro- ductive organs. Any abnormalities in the development and differentiation of these ducts lead to anatomical defects in the female reproductive tract organs categorized as Müllerian duct anomalies. Due to the limited access to fetal tissues, little is understood of human reproductive tract development and the associated anomalies. Although organoids represent a powerful model to decipher human development and disease, such organoids from fetal reproductive organs are not available. Here, we developed organoids from human fetal fallopian tubes and uteri and compared them with their adult counterparts. Our results demonstrate that human fetal reproductive tract epithelia do not express some of the typical markers of adult reproductive tract epithelia. Furthermore, fetal organoids are grossly, histologically, and proteomically different from adult organoids. While external supplementation of WNT ligands or activators in culture medium is an absolute requirement for the adult reproductive tract organoids, fetal organoids are able to grow in WNT-deficient conditions. We also developed decellularized tissue scaffolds from adult human fallopian tubes and uteri. Transplantation of fetal organoids onto these scaffolds led to the regeneration of the adult fallopian tube and uterine epithelia. Importantly, suppression of Wnt signaling, which is altered in patients with Müllerian duct anomalies, inhibits the regenerative ability of human fetal organoids and causes severe anatomical defects in the mouse reproductive tract. Thus, our fetal organoids represent an important platform to study the underlying basis of human female reproductive tract development and diseases.

DOI 10.1073/pnas.2118054119
Citations Scopus - 11Web of Science - 5
Co-authors Pradeep Tanwar, Melissa Tadros, Rebecca Lim
2022 Jamaluddin MFB, Ghosh A, Ingle A, Mohammed R, Ali A, Bahrami M, et al., 'Bovine and human endometrium-derived hydrogels support organoid culture from healthy and cancerous tissues', Proceedings of the National Academy of Sciences, 119 (2022) [C1]
DOI 10.1073/pnas.2208040119
Citations Scopus - 22Web of Science - 3
Co-authors Ayesha Ayesha, Arnab Ghosh, Zamira Gibb, Ajayan Vinu, Gerard Kaiko, Pradeep Tanwar
2022 Jamaluddin MFB, Ko Y-A, Ghosh A, Syed SM, Ius Y, O'Sullivan R, et al., 'Proteomic and functional characterization of intra-tumor heterogeneity in human endometrial cancer', CELL REPORTS MEDICINE, 3 (2022) [C1]
DOI 10.1016/j.xcrm.2022.100738
Citations Scopus - 7Web of Science - 5
Co-authors Shafiq Syed, Arnab Ghosh, Mark Baker, Pradeep Tanwar
2022 Ferdoushi A, Jamaluddin MFB, Li X, Pundavela J, Faulkner S, Hondermarck H, 'Secretome analysis of human schwann cells derived from malignant peripheral nerve sheath tumor', PROTEOMICS, 22 (2022) [C1]
DOI 10.1002/pmic.202100063
Co-authors Hubert Hondermarck, Sam Faulkner
2022 Staudt DE, Murray HC, Skerrett-Byrne DA, Smith ND, Jamaluddin MFB, Kahl RGS, et al., 'Phospho-heavy-labeled-spiketide FAIMS stepped-CV DDA (pHASED) provides real-time phosphoproteomics data to aid in cancer drug selection', CLINICAL PROTEOMICS, 19 (2022) [C1]
DOI 10.1186/s12014-022-09385-7
Citations Scopus - 2Web of Science - 1
Co-authors David Skerrett-Byrne, Nikki Verrills, Ryan Duchatel, Matt Dun, Brett Nixon, Heather Murray
2021 Skerrett-Byrne DA, Bromfield EG, Murray HC, Jamaluddin MFB, Jarnicki AG, Fricker M, et al., 'Time-resolved proteomic profiling of cigarette smoke-induced experimental chronic obstructive pulmonary disease', Respirology, 26 960-973 (2021) [C1]

Background and objective: Chronic obstructive pulmonary disease (COPD) is the third leading cause of illness and death worldwide. Current treatments aim to control symptoms with n... [more]

Background and objective: Chronic obstructive pulmonary disease (COPD) is the third leading cause of illness and death worldwide. Current treatments aim to control symptoms with none able to reverse disease or stop its progression. We explored the major molecular changes in COPD pathogenesis. Methods: We employed quantitative label-based proteomics to map the changes in the lung tissue proteome of cigarette smoke-induced experimental COPD that is induced over 8 weeks and progresses over 12 weeks. Results: Quantification of 7324 proteins enabled the tracking of changes to the proteome. Alterations in protein expression profiles occurred in the induction phase, with 18 and 16 protein changes at 4- and 6-week time points, compared to age-matched controls, respectively. Strikingly, 269 proteins had altered expression after 8 weeks when the hallmark pathological features of human COPD emerge, but this dropped to 27 changes at 12 weeks with disease progression. Differentially expressed proteins were validated using other mouse and human COPD bronchial biopsy samples. Major changes in RNA biosynthesis (heterogeneous nuclear ribonucleoproteins C1/C2 [HNRNPC] and RNA-binding protein Musashi homologue 2 [MSI2]) and modulators of inflammatory responses (S100A1) were notable. Mitochondrial dysfunction and changes in oxidative stress proteins also occurred. Conclusion: We provide a detailed proteomic profile, identifying proteins associated with the pathogenesis and disease progression of COPD establishing a platform to develop effective new treatment strategies.

DOI 10.1111/resp.14111
Citations Scopus - 17Web of Science - 11
Co-authors Michael Fricker, Rodney Scott, Tattjhong Haw, Heather Murray, Elizabeth Bromfield, Matt Dun, Brett Nixon, David Skerrett-Byrne
2021 Ruhen O, Qu X, Jamaluddin MFB, Salomon C, Gandhi A, Millward M, et al., 'Dynamic Landscape of Extracellular Vesicle-Associated Proteins Is Related to Treatment Response of Patients with Metastatic Breast Cancer', MEMBRANES, 11 (2021) [C1]
DOI 10.3390/membranes11110880
Citations Scopus - 4Web of Science - 1
Co-authors Brett Nixon, Matt Dun
2020 Ferdoushi A, Li X, Jamaluddin MFB, Hondermarck H, 'Front Cover: Proteomic Profile of Human Schwann Cells', PROTEOMICS, 20 (2020)
DOI 10.1002/pmic.202070001
2020 Ali A, Syed SM, Jamaluddin MFB, Colino-Sanguino Y, Gallego-Ortega D, Tanwar PS, 'Cell Lineage Tracing Identifies Hormone-Regulated and Wnt-Responsive Vaginal Epithelial Stem Cells', Cell Reports, 30 1463-1477.e7 (2020) [C1]

The intact vaginal epithelium is essential for women's reproductive health and provides protection against HIV and sexually transmitted infections. How this epithelium mainta... [more]

The intact vaginal epithelium is essential for women's reproductive health and provides protection against HIV and sexually transmitted infections. How this epithelium maintains itself remains poorly understood. Here, we used single-cell RNA sequencing (RNA-seq) to define the diverse cell populations in the vaginal epithelium. We show that vaginal epithelial cell proliferation is limited to the basal compartment without any obvious label-retaining cells. Furthermore, we developed vaginal organoids and show that the basal cells have increased organoid forming efficiency. Importantly, Axin2 marks a self-renewing subpopulation of basal cells that gives rise to differentiated cells over time. These cells are ovariectomy-resistant stem cells as they proliferate even in the absence of hormones. Upon hormone supplementation, these cells expand and reconstitute the entire vaginal epithelium. Wnt/ß-catenin is essential for the proliferation and differentiation of vaginal stem cells. Together, these data define heterogeneity in vaginal epithelium and identify vaginal epithelial stem cells.

DOI 10.1016/j.celrep.2020.01.003
Citations Scopus - 32Web of Science - 18
Co-authors Ayesha Ayesha, Pradeep Tanwar, Shafiq Syed
2020 Duchatel RJ, Mannan A, Jackson ER, Staudt D, Skerrett-Byrne DA, Jamaluddin MFB, et al., 'DIPG-29. PHOSPHATIDYLINOSITOL-4,5-BISPHOSPHATE 3-KINASE (PI3K) INHIBITION DRIVES PROTEIN KINASE C ACTIVATION (PKC) IN DIFFUSE INTRINSIC PONTINE GLIOMA (DIPG)', Neuro-oncology, 22 iii292-iii293 (2020)
Co-authors Ryan Duchatel
2020 Feng YC, Liu XY, Teng L, Ji Q, Wu Y, Li JM, et al., 'c-Myc inactivation of p53 through the pan-cancer lncRNA MILIP drives cancer pathogenesis', Nature Communications, 11 (2020) [C1]
DOI 10.1038/s41467-020-18735-8
Citations Scopus - 66Web of Science - 32
Co-authors Yuanyuan Zhang, Rodney Scott, Yuchen Feng, Xu Zhang, Lei Jin
2020 Ferdoushi A, Li X, Griffin N, Faulkner S, Jamaluddin MFB, Gao F, et al., 'Schwann Cell Stimulation of Pancreatic Cancer Cells: A Proteomic Analysis', Frontiers in Oncology, 10 (2020) [C1]
DOI 10.3389/fonc.2020.01601
Citations Scopus - 15Web of Science - 12
Co-authors Chenchen Jiang, Sam Faulkner, Phillip Jobling, Hubert Hondermarck, Dirk Vanhelden, Pradeep Tanwar
2020 Duchatel RJ, Mannan A, Jackson ER, Staudt D, Skerrett-Byrne DA, Jamaluddin MFB, et al., 'DIPG-29. PHOSPHATIDYLINOSITOL-4,5-BISPHOSPHATE 3-KINASE (PI3K) INHIBITION DRIVES PROTEIN KINASE C ACTIVATION (PKC) IN DIFFUSE INTRINSIC PONTINE GLIOMA (DIPG)', Neuro-oncology, 22 iii292-iii293 (2020)
Co-authors Ryan Duchatel
2019 Ferdoushi A, Li X, Bin Jamaluddin MF, Hondermarck H, 'Proteomic Profile of Human Schwann Cells', PROTEOMICS, 20 (2019) [C1]
DOI 10.1002/pmic.201900294
Citations Scopus - 4Web of Science - 4
Co-authors Hubert Hondermarck
2019 Nixon B, De Iuliis GN, Hart HM, Zhou W, Mathe A, Bernstein IR, et al., 'Proteomic profiling of mouse epididymosomes reveals their contributions to post-testicular sperm maturation', Molecular and Cellular Proteomics, 18 S91-S108 (2019) [C1]
DOI 10.1074/mcp.RA118.000946
Citations Scopus - 114Web of Science - 83
Co-authors Andrea Johns, Elizabeth Bromfield, Brett Nixon, David Skerrett-Byrne, Matt Dun, Geoffry DeiuliIs
2019 Al-Juboori AAA, Ghosh A, Bin Jamaluddin MF, Kumar M, Sahoo SS, Syed SM, et al., 'Proteomic Analysis of Stromal and Epithelial Cell Communications in Human Endometrial Cancer Using a Unique 3D Co-Culture Model', PROTEOMICS, 19 (2019) [C1]
DOI 10.1002/pmic.201800448
Citations Scopus - 12Web of Science - 10
Co-authors Shafiq Syed, Pradeep Tanwar, Arnab Ghosh
2019 Jamaluddin MFB, Nagendra PB, Nahar P, Oldmeadow C, Tanwar PS, 'Proteomic Analysis Identifies Tenascin-C Expression Is Upregulated in Uterine Fibroids', REPRODUCTIVE SCIENCES, 26 476-486 (2019) [C1]
DOI 10.1177/1933719118773420
Citations Scopus - 6Web of Science - 3
Co-authors Christopher Oldmeadow, Pradeep Tanwar
2018 Goad J, Ko Y-A, Kumar M, Jamaluddin MFB, Tanwar PS, 'Oestrogen fuels the growth of endometrial hyperplastic lesions initiated by overactive Wnt/ß-catenin signalling.', Carcinogenesis, 39 1105-1116 (2018) [C1]
DOI 10.1093/carcin/bgy079
Citations Scopus - 20Web of Science - 14
Co-authors Pradeep Tanwar
2018 Ko YA, Jamaluddin MFB, Adebayo M, Bajwa P, Scott RJ, Dharmarajan AM, et al., 'Extracellular matrix (ECM) activates ß-catenin signaling in uterine fibroids', Reproduction, 155 61-71 (2018) [C1]

Recent studies showed that genetic aberrations in the MED12 gene, probably through the canonical WNT/ß-catenin pathway, lead to the pathogenesis of uterine fibroids. However, a co... [more]

Recent studies showed that genetic aberrations in the MED12 gene, probably through the canonical WNT/ß-catenin pathway, lead to the pathogenesis of uterine fibroids. However, a comprehensive analysis of the WNT pathway in MED12-mutated and MED12-wildtype fibroids has not been performed. The objective of this study was to determine the status of the WNT pathway in human fibroids. We performed Sanger sequencing to define the MED12 mutational status of fibroids and normal myometrium samples. qPCR arrays were carried out to determine the status of the WNT signaling pathway in MED12-mutated and MED12-wild-type fibroids. Liquid chromatography-mass spectrometry (LC-MS), Western blotting and immunohistochemistry were used to monitor the expression of ß-catenin. We showed that ß-catenin expression was increased in fibroids compared to the adjacent myometrium samples. However, ß-catenin expression showed no correlation with MED12 mutation status. Of all the WNT signaling components, WNT inhibitors showed the greatest differences in expression between fibroids and controls. WIF1, a WNT inhibitor, was identified as the most significantly upregulated gene in fibroids. We cultured primary fibroid cells on hydrogels of known stiffness to decipher the influence of biomechanical cues on ß-catenin expression and revealed increased levels of ß-catenin when cells were cultured on a stiffer surface. In conclusion, our data showed that ß-catenin expression in fibroids occurs independently of MED12 mutations. Biomechanical changes upregulate ß-catenin expression in fibroids, providing an attractive avenue for developing new treatments for this disease.

DOI 10.1530/REP-17-0339
Citations Scopus - 30Web of Science - 18
Co-authors Rodney Scott, Pradeep Tanwar
2018 Jamaluddin MFB, Nahar P, Tanwar PS, 'Proteomic characterization of the extracellular matrix of human uterine fibroids', Endocrinology, 159 2656-2669 (2018) [C1]

Uterine leiomyomas (fibroids) are the most common benign tumors that are associated with increased production of extracellular matrix (ECM). Excessive ECM deposition plays a major... [more]

Uterine leiomyomas (fibroids) are the most common benign tumors that are associated with increased production of extracellular matrix (ECM). Excessive ECM deposition plays a major role in the enlargement and stiffness of these tumors and contributes to clinical symptoms, such as abnormal bleeding and abdominal pain. However, no study so far has explored the global composition of the ECM of fibroids and normal myometrium. In this study, we performed a systematic ECM enrichment procedure and comparative proteomic analyses to profile the ECM composition of genetically annotated different-sized fibroids (small, medium, and large) and adjacent normal myometrium (ANM). Our matrisome analysis identified a combined total of 108, 126, 126, and 130 unique ECM and ECM-associated proteins with a confidence corresponding to a false discovery rate,1%inANM and in small, medium, and large fibroids, respectively. The majority of fibroid ECM proteins belong to the core matrisome that includes glycoproteins, collagens, and proteoglycans. Considering that the small-sized fibroids represent the initial stages of leiomyogenesis, we highlighted some of the most abundant and important upregulated ECM proteins in small fibroids (i.e., POSTN, TNC, COL3A1, COL24A1, and ASPN). Furthermore, we revealed 30 unique ECM proteins that exist only in fibroids but that are not present in ANM regardless of MED12 mutation. We propose that some of the proteins identified represent potential novel ECM drug targets that may change the paradigm of fibroid treatment.

DOI 10.1210/en.2018-00151
Citations Scopus - 24Web of Science - 17
Co-authors Pradeep Tanwar
2018 Jamaluddin MFB, Ko YA, Kumar M, Brown Y, Bajwa P, Nagendra PB, et al., 'Proteomic profiling of human uterine fibroids reveals upregulation of the extracellular matrix protein periostin', Endocrinology, 159 1106-1118 (2018) [C1]

The central characteristic of uterine fibroids is excessive deposition of extracellular matrix (ECM), which contributes to fibroid growth and bulk-type symptoms. Despite this, ver... [more]

The central characteristic of uterine fibroids is excessive deposition of extracellular matrix (ECM), which contributes to fibroid growth and bulk-type symptoms. Despite this, very little is known about patterns of ECM protein expression in fibroids and whether these are influenced by the most common genetic anomalies, which relate to MED12. We performed extensive genetic and proteomic analyses of clinically annotated fibroids and adjacent normal myometrium to identify the composition and expression patterns of ECM proteins in MED12 mutation-positive and mutation-negative uterine fibroids. Genetic sequencing of tissue samples revealed MED12 alterations in 39 of 65 fibroids (60%) from 14 patients. Using isobaric tagged-based quantitative mass spectrometry on three selected patients (n = 9 fibroids), we observed a common set of upregulated (.1.5-fold) and downregulated (,0.66-fold) proteins in small, medium, and large fibroid samples of annotated MED12 status. These two sets of upregulated and downregulated proteins were the same in all patients, regardless of variations in fibroid size and MED12 status. We then focused on one of the significant upregulated ECM proteins and confirmed the differential expression of periostin using western blotting and immunohistochemical analysis. Our study defined the proteome of uterine fibroids and identified that increased ECM protein expression, in particular periostin, is a hallmark of uterine fibroids regardless of MED12 mutation status. This study sets the foundation for further investigations to analyze the mechanisms regulating ECM overexpression and the functional role of upregulated ECM proteins in leiomyogenesis.

DOI 10.1210/en.2017-03018
Citations Scopus - 16Web of Science - 11
Co-authors Pradeep Tanwar, David Skerrett-Byrne, Hubert Hondermarck, Mark Baker, Rodney Scott, Matt Dun
2014 Jamaluddin MFB, Bailey UM, Schulz BL, 'Oligosaccharyltransferase subunits bind polypeptide substrate to locally enhance N-glycosylation', Molecular and Cellular Proteomics, 13 3286-3293 (2014)

Oligosaccharyltransferase is a multiprotein complex that catalyzes asparagine-linked glycosylation of diverse proteins. Using yeast genetics and glycoproteomics, we found that tra... [more]

Oligosaccharyltransferase is a multiprotein complex that catalyzes asparagine-linked glycosylation of diverse proteins. Using yeast genetics and glycoproteomics, we found that transient interactions between nascent polypeptide and Ost3p/Ost6p, homologous subunits of oligosaccharyltransferase, were able to modulate glycosylation efficiency in a site-specific manner in vivo. These interactions were driven by hydrophobic and electrostatic complementarity between amino acids in the peptidebinding groove of Ost3p/Ost6p and the sequestered stretch of substrate polypeptide. Based on this dependence, we used in vivo scanning mutagenesis and in vitro biochemistry to map the precise interactions that affect site-specific glycosylation efficiency. We conclude that transient binding of substrate polypeptide by Ost3p/Ost6p increases glycosylation efficiency at asparagines proximal and C-terminal to sequestered sequences. We detail a novel mode of interaction between translocating nascent polypeptide and oligosaccharyltransferase in which binding to Ost3p/Ost6p segregates a short flexible loop of glycosylation-competent polypeptide substrate that is delivered to the oligosaccharyltransferase active site for efficient modification.

DOI 10.1074/mcp.M114.041178
Citations Scopus - 12Web of Science - 12
2014 Tan NY, Bailey UM, Jamaluddin MF, Mahmud SHB, Raman SC, Schulz BL, 'Sequence-based protein stabilization in the absence of glycosylation', Nature Communications, 5 (2014)

Asparagine-linked N-glycosylation is a common modification of proteins that promotes productive protein folding and increases protein stability. Although N-glycosylation is import... [more]

Asparagine-linked N-glycosylation is a common modification of proteins that promotes productive protein folding and increases protein stability. Although N-glycosylation is important for glycoprotein folding, the precise sites of glycosylation are often not conserved between protein homologues. Here we show that, in Saccharomyces cerevisiae, proteins upregulated during sporulation under nutrient deprivation have few N-glycosylation sequons and in their place tend to contain clusters of like-charged amino-acid residues. Incorporation of such sequences complements loss of in vivo protein function in the absence of glycosylation. Targeted point mutation to create such sequence stretches at glycosylation sequons in model glycoproteins increases in vitro protein stability and activity. A dependence on glycosylation for protein stability or activity can therefore be rescued with a small number of local point mutations, providing evolutionary flexibility in the precise location of N-glycans, allowing protein expression under nutrient-limiting conditions, and improving recombinant protein production. © 2014 Macmillan Publishers Limited. All rights reserved.

DOI 10.1038/ncomms4099
Citations Scopus - 27Web of Science - 26
2013 Mohd Yusuf SNH, Bailey UM, Tan NY, Jamaluddin MF, Schulz BL, 'Mixed disulfide formation in vitro between a glycoprotein substrate and yeast oligosaccharyltransferase subunits Ost3p and Ost6p', Biochemical and Biophysical Research Communications, 432 438-443 (2013)

Oligosaccharyltransferase (OTase) glycosylates selected asparagine residues in secreted and membrane proteins in eukaryotes, and asparagine (N)-glycosylation affects the folding, ... [more]

Oligosaccharyltransferase (OTase) glycosylates selected asparagine residues in secreted and membrane proteins in eukaryotes, and asparagine (N)-glycosylation affects the folding, stability and function of diverse glycoproteins. The range of acceptor protein substrates that are efficiently glycosylated depends on the action of several accessory subunits of OTase, including in yeast the homologous proteins Ost3p and Ost6p. A model of Ost3p and Ost6p function has been proposed in which their thioredoxin-like active site cysteines form transient mixed disulfide bonds with cysteines in substrate proteins to enhance the glycosylation of nearby asparagine residues. We tested aspects of this model with a series of in vitro assays. We developed a whole protein mixed disulfide interaction assay that showed that Ost6p could form mixed disulfide bonds with selected cysteines in pre-reduced yeast Gas1p, a model glycoprotein substrate of Ost3p and Ost6p. A complementary peptide affinity chromatography assay for mixed disulfide bond formation showed that Ost3p could also form mixed disulfide bonds with cysteines in selected reduced tryptic peptides from Gas1p. Together, these assays showed that the thioredoxin-like active sites of Ost3p and Ost6p could form transient mixed disulfide bonds with cysteines in a model substrate glycoprotein, consistent with the function of Ost3p and Ost6p in modulating N-glycosylation substrate selection by OTase in vivo. © 2013 Elsevier Inc.

DOI 10.1016/j.bbrc.2013.01.128
Citations Scopus - 14Web of Science - 14
2012 Bailey U-M, Jamaluddin MF, Schulz BL, 'Analysis of Congenital Disorder of Glycosylation-Id in a Yeast Model System Shows Diverse Site-Specific Under-glycosylation of Glycoproteins', JOURNAL OF PROTEOME RESEARCH, 11 5376-5383 (2012)
DOI 10.1021/pr300599f
Citations Scopus - 39Web of Science - 40
2011 Jamaluddin MFB, Bailey U-M, Tan NYJ, Stark AP, Schulz BL, 'Polypeptide binding specificities of Saccharomyces cerevisiae oligosaccharyltransferase accessory proteins Ost3p and Ost6p', PROTEIN SCIENCE, 20 849-855 (2011)
DOI 10.1002/pro.610
Citations Scopus - 20Web of Science - 20
Show 29 more journal articles

Conference (14 outputs)

Year Citation Altmetrics Link
2023 Duchatel R, Jackson E, Parackal S, Sun C, Daniel P, Mannan A, et al., 'EXPLOITING THE GENETIC DEPENDENCY ON PI3K/ MTOR SIGNALING FOR THE TREATMENT OF H3-ALTERED DIFFUSE MIDLINE GLIOMA', NEURO-ONCOLOGY, CANADA, Vancouver (2023)
Co-authors Ryan Duchatel, Murray Cairns, Brett Nixon, Matt Dun, Susan Hua, David Skerrett-Byrne
2022 Burns GL, Hoedt EC, Jamaluddin MFB, Shanahan E, Lim Y, Teh JJ, et al., 'Seroreactivity to mucosa associated microbiota is associated with T cell gut-homing in functional dyspepsia patients (Withdrawal of Vol 36, 10.1096/FASEBJ.2022.36.S1.R4212, 2022)', FASEB JOURNAL (2022)
DOI 10.1096/fasebj.2022.36.S1.R4212
Citations Web of Science - 1
Co-authors Marjorie Walker, G Burns, Martin Veysey, Jay Horvat, Emily Hoedt, Simon Keely
2022 Burns GL, Hoedt EC, Jamaluddin MF, Shanahan ER, Lim Y, Teh JJ, et al., 'FUNCTIONAL DYSPEPSIA PATIENTS HAVE IGG ANTIBODIES AGAINST A NOVEL ISOLATE OF STREPTOCOCCUS SALIVARIUS', GASTROENTEROLOGY, San Diego, CA (2022)
Co-authors Marjorie Walker, Jay Horvat, Martin Veysey, Simon Keely, G Burns, Nicholas Talley, Matt Dun, Emily Hoedt
2021 Barreto DES, Murray H, Skerrett-Byrne D, Kahl R, Duchatel R, Jamaluddin M, et al., 'Phosphoproteomics predicts novel treatment targets for FLT3-ITD+ AML resistant to targeted therapy', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2021)
Co-authors David Skerrett-Byrne, Heather Murray
2020 Duchatel RJ, Jackson ER, Mannan A, Staudt D, Skerrett-Byrne DA, Nixon B, et al., 'Targeting phosphatidylinositol-4,5-bisphosphate 3-kinase (PI3K) and protein kinase C (PKC) activation in diffuse midline glioma (DMG)', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2020)
Co-authors Brett Nixon, Matt Dun, David Skerrett-Byrne
2020 Staudt D, Kahl R, Skerrett-Byrne D, Murray H, Jamaluddin M, Woldu AS, et al., 'Proteomic and phosphoproteomic profiling of wildtype (-WT and -FL) and mutant FLT3 (-ITD,-D835V/Y, -and ITD/D835V/Y) signaling pathways in acute myeloid leukemia', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2020)
Co-authors Anoop Enjeti, Heather Murray, David Skerrett-Byrne, Matt Dun, Nikki Verrills
2020 Duchatel RJ, Mannan A, Jackson ER, Staudt D, Skerrett-Byrne DA, Jamaluddin MFB, et al., 'PHOSPHATIDYLINOSITOL-4,5-BISPHOSPHATE 3-KINASE (PI3K) INHIBITION DRIVES PROTEIN KINASE C ACTIVATION (PKC) IN DIFFUSE INTRINSIC PONTINE GLIOMA (DIPG)', NEURO-ONCOLOGY (2020)
Co-authors David Skerrett-Byrne, Matt Dun
2019 Duchatel RJ, Jackson ER, Staudt D, Skerrett-Byrne DA, Jamaluddin MFB, Germon Z, et al., 'Keynote Speakers', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2019)
DOI 10.1111/ajco.13253
Co-authors Matt Dun, David Skerrett-Byrne
2019 Brown Y, Ghosh A, Venkata VD, Jamaluddin MFB, Ali A, Tanwar PS, 'Enter the Matrix to Uncover Potential New Biomarkers for the Initial Stages of Ovarian Cancer Development', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2019)
Co-authors Arnab Ghosh, Pradeep Tanwar
2019 Jamaluddin M, Ko Y-A, Syed S, Ius Y, O'Sullivan R, Netherton J, et al., 'Understanding the basis of intra-tumour heterogeneity in human endometrial cancer', Newcastle City Hall, Newcastle, NSW, Australia (2019)
Co-authors Pradeep Tanwar, Shafiq Syed, Mark Baker
2018 Brown Y, Jamaluddin MFB, Ghosh A, Mellick AS, Murtha L, Boyle A, Tanwar PS, 'The Glue of Cancer Cell Life: Characterization of the Acellular Component of High Grade Serous Ovarian Cancer Identifies Potential Novel Drug Targets', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2018)
Co-authors Arnab Ghosh, Lucy Murtha, Pradeep Tanwar
2018 Jamaluddin MFB, Ko Y-A, Ius Y, O'Sullivan R, Nahar P, Jaaback K, Tanwar PS, 'Why Targeted Therapies Don't Work?: Proteomic Characterization of Intratumor Heterogeneity of Human Endometrial Cancer', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2018)
Co-authors Pradeep Tanwar
2018 Gould T, Jamaluddin MFB, Pockney P, Dun M, 'Quantitative Proteomics for the Early Detection of Colorectal Cancer', ASIA-PACIFIC JOURNAL OF CLINICAL ONCOLOGY (2018)
Co-authors Peter Pockney, Matt Dun
2017 Yi-An K, Jamaluddin M, Tanwar PS, 'Extracellular Matrix (ECM) and Wnt signalling nexus in human uterine leiomyomas', Perth (2017)
Co-authors Pradeep Tanwar
Show 11 more conferences

Preprint (2 outputs)

Year Citation Altmetrics Link
2023 Duchatel R, Jackson E, Parackal S, Sun C, Daniel P, Mannan A, et al., 'PI3K/mTOR is a therapeutically targetable genetic dependency in diffuse intrinsic pontine glioma (2023)
DOI 10.1101/2023.04.17.537256
Co-authors Susan Hua, Matt Dun, Murray Cairns, Lizzie Manning, Heather Murray, Ryan Duchatel, Brett Nixon, David Skerrett-Byrne
2022 Staudt D, Murray H, Skerrett-Byrne D, Smith N, Jamaluddin M, Kahl RGS, et al., 'High-Throughput Global Phosphoproteomic Profiling Using Phospho Heavy-Labeled-Spiketide FAIMS Stepped-CV DDA (pHASED) (2022)
DOI 10.1101/2022.04.22.489124
Co-authors David Skerrett-Byrne, Matt Dun

Thesis / Dissertation (1 outputs)

Year Citation Altmetrics Link
2015 Jamaluddin M, Molecular mechanisms regulating N-glycosylation site selection by yeast oligosaccharyltransferase: Role of Ost3p and Ost6p, The University of Queensland (2015)
DOI 10.14264/uql.2015.362
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Grants and Funding

Summary

Number of grants 14
Total funding $882,720

Click on a grant title below to expand the full details for that specific grant.


20233 grants / $14,300

A blood test for endometrial cancer$7,739

Funding body: Cancer Detection and Therapy Small Pilot Project Funding 2023

Funding body Cancer Detection and Therapy Small Pilot Project Funding 2023
Project Team

Dr Muhammad Fairuz Jamaluddin, Dr Hruda Malik, Dr Mamta Pariyar, Prof Pradeep Tanwar

Scheme Hunter Medical Research Institute
Role Lead
Funding Start 2023
Funding Finish 2023
GNo
Type Of Funding Internal
Category INTE
UON N

Cancer Detection and Therapy Research Program Equipment Maintenance$3,935

Funding body: Hunter Medical Research Institute (HMRI)

Funding body Hunter Medical Research Institute (HMRI)
Project Team

Dr Muhammad Fairuz Jamaluddin, Prof Pradeep Tanwar

Scheme Hunter Medical Research Institute
Role Lead
Funding Start 2023
Funding Finish 2023
GNo
Type Of Funding Internal
Category INTE
UON N

Ascites-derived organoid based drug screening for a personalized treatment in a high-grade serous ovarian cancer (HGSOC) patient$2,627

Funding body: Cancer Detection and Therapy EMCR Shovel-Ready Project Funding

Funding body Cancer Detection and Therapy EMCR Shovel-Ready Project Funding
Project Team

Dr Mamta Pariyar, Dr Hiren Mandaliya, Dr Muhammad Fairuz Jamaluddin, Prof Pradeep Tanwar

Scheme Hunter Medical Research Institute
Role Investigator
Funding Start 2023
Funding Finish 2023
GNo
Type Of Funding Internal
Category INTE
UON N

20211 grants / $15,000

Development of a diagnostic and prognostic blood-based test for endometriosis$15,000

Funding body: College of Health, Medicine and Wellbeing, UoN

Funding body College of Health, Medicine and Wellbeing, UoN
Project Team

Dr Shafiq Syed, Dr Arnab Ghosh, Dr Muhammad Jamaluddin, Dr Manish Kumar, Professor Pradeep Tanwar, Dr Pravin Nahar, Dr Ken Jaaback

Scheme 2021 Strategic Research Pilot Grants
Role Investigator
Funding Start 2021
Funding Finish 2021
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

20201 grants / $4,550

Engineering of bio-inspired gel from patient-derived tumour samples for personalized medicine$4,550

Funding body: 2020 Faculty Strategic Pilot Grant

Funding body 2020 Faculty Strategic Pilot Grant
Project Team

Dr Muhammad Fairuz Jamaluddin, Assoc Prof Pradeep Tanwar, Assoc Prof Ajay Karakoti, Prof Ajayan Vinu

Scheme 2020 Faculty of Health and Medicine Strategic Pilot Grant
Role Lead
Funding Start 2020
Funding Finish 2020
GNo
Type Of Funding Other Public Sector - Local
Category 2OPL
UON N

20195 grants / $734,563

Defining the roles of hormones in the pathogenesis of ovarian cancer$566,277

Funding body: Ovarian Cancer Research Foundation (OCRF)

Funding body Ovarian Cancer Research Foundation (OCRF)
Project Team Professor Pradeep Tanwar, Doctor Muhammad Fairuz Jamaluddin, Prof Arunasalam Dharmarajan
Scheme Research Grant
Role Investigator
Funding Start 2019
Funding Finish 2021
GNo G1900444
Type Of Funding C3200 – Aust Not-for Profit
Category 3200
UON Y

Endometrial Cancer Research Project$96,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Pradeep Tanwar, Doctor Shafiq Syed, Doctor Muhammad Fairuz Jamaluddin
Scheme Project Grant
Role Investigator
Funding Start 2019
Funding Finish 2019
GNo G1900346
Type Of Funding C3300 – Aust Philanthropy
Category 3300
UON Y

Microinjection workstation to facilitate disease modelling in organoids$47,862

Funding body: NHMRC (National Health & Medical Research Council)

Funding body NHMRC (National Health & Medical Research Council)
Project Team Professor Pradeep Tanwar, Professor Xu Dong Zhang, Associate Professor Lei Jin, Professor Hubert Hondermarck, Associate Professor Susan Hua, Doctor Muhammad Fairuz Jamaluddin
Scheme Equipment Grant
Role Investigator
Funding Start 2019
Funding Finish 2019
GNo G1900304
Type Of Funding Scheme excluded from IGS
Category EXCL
UON Y

Proteomic characterization of human uterine fibroids harbouring co-existing MED12 and FH in Australian women$20,063

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Muhammad Fairuz Jamaluddin, Professor Pradeep Tanwar, Doctor Pravin Nahar
Scheme Research Grant
Role Lead
Funding Start 2019
Funding Finish 2019
GNo G1900225
Type Of Funding C2400 – Aust StateTerritoryLocal – Other
Category 2400
UON Y

Temperature regulated incubator shaker$4,361

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Pradeep Tanwar, Doctor Mahesh Kumar, Doctor Muhammad Fairuz Jamaluddin
Scheme Early and Mid-Career Equipment Grant
Role Investigator
Funding Start 2019
Funding Finish 2019
GNo G1900105
Type Of Funding C3300 – Aust Philanthropy
Category 3300
UON Y

20183 grants / $94,307

Non-invasive detection of DIPG specific DNA and protein using sequential blood collections$57,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Matt Dun, Doctor Muhammad Fairuz Jamaluddin, Doctor Ryan Duchatel, Doctor Frank Alvaro
Scheme Project Grant
Role Investigator
Funding Start 2018
Funding Finish 2020
GNo G1801235
Type Of Funding C3300 – Aust Philanthropy
Category 3300
UON Y

Hormonal control of ovarian cancer$20,000

Funding body: Hunter Medical Research Institute

Funding body Hunter Medical Research Institute
Project Team Professor Pradeep Tanwar, Ms Janine Lombard, Doctor Hiren Mandaliya, Doctor Manish Kumar Jhamb, Doctor Muhammad Fairuz Jamaluddin
Scheme Project Grant
Role Investigator
Funding Start 2018
Funding Finish 2018
GNo G1801351
Type Of Funding C3300 – Aust Philanthropy
Category 3300
UON Y

Periostin as a biomarker in the diagnosis and surveillance of uterine leiomyomas$17,307

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Muhammad Fairuz Jamaluddin, Professor Pradeep Tanwar, Doctor Pravin Nahar
Scheme Research Grant
Role Lead
Funding Start 2018
Funding Finish 2018
GNo G1800008
Type Of Funding C3200 – Aust Not-for Profit
Category 3200
UON Y

20171 grants / $20,000

Mediator complex subunit 12 (MED12) gene in pathogenesis of uterine smooth muscle tumours$20,000

Funding body: John Hunter Hospital Charitable Trust

Funding body John Hunter Hospital Charitable Trust
Project Team Doctor Muhammad Fairuz Jamaluddin, Professor Pradeep Tanwar, Doctor Pravin Nahar
Scheme Research Grant
Role Lead
Funding Start 2017
Funding Finish 2017
GNo G1700368
Type Of Funding C3200 – Aust Not-for Profit
Category 3200
UON Y
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Research Supervision

Number of supervisions

Completed1
Current13

Current Supervision

Commenced Level of Study Research Title Program Supervisor Type
2023 PhD Developing an Early Detection and Prognostic Test for Ovarian Cancer PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2023 PhD Patient Derive Organoid as a Model for Drug Screening in Women Suffering from Endometriosis PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2023 PhD Role Of Stem/Progenitor Cells In Endometrial Biology And Carcinogenesis PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2023 PhD Patient-derived Organoids for Gynaecological Diseases PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2023 PhD Patient Derive Organoid As A Model For Drug Screening In Women Suffering From Endometrial Cancer PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2023 PhD Role of Extracellular Matrix in Gynaecological Diseases PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2023 PhD Using Preclinical Models to Improve Outcomes for Gynaecological Diseases – Endometrial Organoid to Study Drug Resistance in Gynaecological Diseases PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2022 PhD Using Patient-Derived Models to Understand the Pathobiology of Gynaecological Diseases PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2022 PhD Comparative Proteomic Analysis of the Organoids from Endometriosis Patients with the Organoids from Normal Endometrium and Endometrial Cancer PhD (Medical Genetics), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2022 PhD Development and Characterization of Endometrial Organoids PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2022 PhD Using OMICS based Approaches for Personalizing Treatments for Gynecological Cancer Patients PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2021 PhD An Organoid-Based Drug Screening for Gynaecological Diseases PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor
2020 PhD Developing Patient-Derived Ovarian Cancer Organoids as a Model for High Throughput Drug Screening and Personalised Medicine PhD (Medical Biochemistry), College of Health, Medicine and Wellbeing, The University of Newcastle Co-Supervisor

Past Supervision

Year Level of Study Research Title Program Supervisor Type
2019 Honours The role of endometrial stem cells in the origin of ovarian cancer Biochemistry & Cell Biology, School of Biomedical Sciences and Pharmacy, Faculty of Health and Medicine, University of Newcastle Co-Supervisor
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Dr Muhammad Fairuz Jamaluddin

Position

Associate Lecturer
School of Biomedical Sciences and Pharmacy
College of Health, Medicine and Wellbeing

Contact Details

Email muhammad.jamaluddin@newcastle.edu.au
Phone (02) 4921 7476
Links Research Networks
Google+
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